Long non‐coding <scp>RNA</scp>TDRG1 aggravates colorectal cancer stemness by binding with miR‐873‐5p to upregulate PRKAR2

Hong, Qingqi; Mai, Peishan; Wu, Bin; Wang, Haibin; Xiao, Mingzhe; You, Jianbin

doi:10.1002/tox.23602

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…TDRG1 levels are significantly upregulated in 3D non-adherent spheroids derived from parental CRC cells. Further studies indicate that knockdown of TDRG1 inhibits the stemness of CRC cells ( 196 ).…”

Section: Lncrnas Regulate Cancer Cell Stemnessmentioning

confidence: 99%

The functions and mechanisms of long non-coding RNA in colorectal cancer

Lin,

Zhao,

et al. 2024

Front. Oncol.

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CRC poses a significant challenge in the global health domain, with a high number of deaths attributed to this disease annually. If CRC is detected only in its advanced stages, the difficulty of treatment increases significantly. Therefore, biomarkers for the early detection of CRC play a crucial role in improving patient outcomes and increasing survival rates. The development of a reliable biomarker for early detection of CRC is particularly important for timely diagnosis and treatment. However, current methods for CRC detection, such as endoscopic examination, blood, and stool tests, have certain limitations and often only detect cases in the late stages. To overcome these constraints, researchers have turned their attention to molecular biomarkers, which are considered a promising approach to improving CRC detection. Non-invasive methods using biomarkers such as mRNA, circulating cell-free DNA, microRNA, LncRNA, and proteins can provide more reliable diagnostic information. These biomarkers can be found in blood, tissue, stool, and volatile organic compounds. Identifying molecular biomarkers with high sensitivity and specificity for the early and safe, economic, and easily measurable detection of CRC remains a significant challenge for researchers.

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Section: Lncrnas Regulate Cancer Cell Stemnessmentioning

confidence: 99%

The functions and mechanisms of long non-coding RNA in colorectal cancer

Lin,

Zhao,

et al. 2024

Front. Oncol.

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“…Colorectal cancer, a common digestive tract tumor that mainly resulted from colonic mucosa epithelium, ranks the third of cancer‐related deaths all over the world 1–4 . Colorectal cancer greatly threatened the health of patients with the increasing morbidity year by year and high mortality 5 .…”

Section: Introductionmentioning

confidence: 99%

Matrine restrains the development of colorectal cancer through regulating the AGRN/Wnt/β‐catenin pathway

Wen

et al. 2023

Environmental Toxicology

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Background Colorectal cancer is a common malignant digestive tract tumor. This study aimed to explore the biological role and potential underlying mechanism of matrine in colorectal cancer. Methods The mRNA expression of AGRN was measured using RT‐qPCR. Cell proliferation, migration, invasion and apoptosis were determined using CCK‐8, EdU, transwell assays and flow cytometry, respectively. Xenograft tumor experiment was performed to explore the action of matrine and AGRN on tumor growth in colorectal cancer in vivo. Immunohistochemistry (IHC) assay was applied for AGRN, β‐catenin, and c‐Myc expression in the tumor tissues from mice. Results Matrine dramatically repressed cell growth and reduced the level of AGRN in colorectal cancer cells. AGRN expression was boosted colorectal cancer tissues and cells. AGRN downregulation depressed cell proliferation, migration, invasion, and enhanced cell apoptosis in colorectal cancer cells. Moreover, matrine showed the anti‐tumor effects on colorectal cancer cells via regulating AGRN expression. AGRN knockdown could inactivate the Wnt/β‐catenin pathway in colorectal cancer cells. We found that AGRN downregulation exhibited the inhibition action in the progression of colorectal cancer by modulating the Wnt/β‐catenin pathway. In addition, matrine could inhibit the activation of the Wnt/β‐catenin pathway through regulating AGRN in colorectal cancer cells. Furthermore, xenograft tumor experiment revealed that matrine treatment or AGRN knockdown repressed the development of colorectal cancer via the Wnt/β‐catenin pathway in vivo. Conclusion Matrine retarded colorectal cancer development by modulating AGRN to inactivate the Wnt/β‐catenin pathway.

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